Comprehensive Guide to Coronary Artery Disease (CAD) for Nursing and Health Students : Nursing Care Plan:

Coronary Artery Disease (CAD)

A detailed overview for nursing/health sciences students

1. Introduction

Coronary Artery Disease (CAD), also called Ischemic Heart Disease (IHD) or Coronary Heart Disease (CHD), is a condition in which the coronary arteries (the blood vessels that supply the heart muscle) become narrowed or blocked, usually due to atherosclerosis. This reduces blood flow and oxygen supply to the myocardium, leading to myocardial ischemia and, if severe or prolonged, myocardial infarction (heart attack).

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CAD is one of the leading causes of morbidity and mortality worldwide. It is a chronic, progressive disease that often begins silently years before symptoms appear. CAD may present as:

Stable angina (predictable chest pain with exertion or stress)
Unstable angina
Myocardial infarction (ST-elevation MI, non-ST elevation MI)
Silent ischemia (ischemia without obvious symptoms)
Sudden cardiac death

From a nursing perspective, CAD is central to cardiovascular practice. Nurses are deeply involved in prevention, acute care, rehabilitation, and long-term management, making a thorough understanding of the disease essential.

2. Causes and Pathophysiology

2.1 Primary cause: Atherosclerosis

The main underlying cause of CAD is atherosclerosis—deposition of lipids, inflammatory cells, and fibrous tissue in the intima of coronary arteries, forming atherosclerotic plaques.

Key steps:

Endothelial injury/dysfunction
Factors like hypertension, smoking, high LDL cholesterol, diabetes, and systemic inflammation damage the endothelium (inner lining of arteries). This causes:

Increased permeability to lipoproteins
Decreased nitric oxide (NO) production (less vasodilation)
Increased expression of adhesion molecules (promotes inflammation)

Lipid accumulation and inflammation

LDL cholesterol infiltrates the arterial wall and becomes oxidized.
Monocytes adhere to the endothelium, migrate into the intima, and become macrophages.
Macrophages engulf oxidized LDL, turning into foam cells. Clusters of foam cells form fatty streaks.

Plaque formation

Smooth muscle cells migrate from the media to the intima, proliferate, and secrete extracellular matrix (collagen, proteoglycans).
A fibrous cap forms over a lipid-rich necrotic core, creating a fibro-fatty plaque.

Plaque progression and complications

Progressive plaque growth narrows the lumen, limiting blood flow, especially during increased oxygen demand (exercise, stress), resulting in stable angina.
Plaques can become unstable: thin fibrous cap, large lipid core, heavy inflammatory infiltration.
Plaque rupture or erosion exposes thrombogenic material, causing acute thrombus formation which may partially or completely occlude the artery. This leads to:

Unstable angina (UA)
Non-ST elevation MI (NSTEMI)
ST elevation MI (STEMI)

2.2 Other, less common causes

While atherosclerosis is the main cause, CAD can also result from:

Coronary artery spasm (Prinzmetal/variant angina)
Coronary artery embolism (e.g., from infective endocarditis, atrial fibrillation)
Coronary artery dissection (spontaneous coronary artery dissection, often in younger women)
Congenital coronary anomalies
Vasculitis (e.g., Kawasaki disease)
Radiation-induced coronary disease

3. Predisposing Factors (Risk Factors)

CAD is multifactorial. Risk factors are usually divided into non-modifiable and modifiable.

3.1 Non-modifiable risk factors

Age

Risk increases with age; men over 45 and women over 55 have higher risk.

Sex

Men develop CAD earlier than women.
After menopause, women’s risk approaches that of men.

Family history/genetics

First-degree relative (parent, sibling) with premature CAD (men <55, women <65) increases risk.
Certain genetic lipid disorders (e.g., familial hypercholesterolemia).

Ethnicity

Some groups (e.g., South Asians, African ancestry in some regions) have higher CAD risk.

3.2 Modifiable risk factors

Dyslipidemia

High LDL cholesterol
Low HDL cholesterol
High triglycerides
Elevated non-HDL cholesterol
Dyslipidemia accelerates atherogenesis.

Hypertension

Chronic high blood pressure damages endothelium, promotes plaque formation, and increases myocardial workload.

Diabetes mellitus / Prediabetes

Both type 1 and type 2 diabetes significantly increase CAD risk.
Associated with low HDL, high triglycerides, endothelial dysfunction, and inflammation.

Cigarette smoking

Causes endothelial damage, increased clotting tendency, decreased oxygen delivery, and increased heart rate and blood pressure.
Both active and passive smoking increase risk.

Obesity and central (abdominal) obesity

Associated with insulin resistance, dyslipidemia, hypertension, chronic low-grade inflammation.

Physical inactivity

Lack of regular aerobic exercise is linked with obesity, poor lipid profile, and insulin resistance.

Unhealthy diet

High intake of saturated fats, trans fats, refined carbohydrates, sugar-sweetened beverages, and excess salt.
Low intake of fruits, vegetables, whole grains, and omega-3 fatty acids.

Psychosocial factors

Chronic stress, depression, social isolation, low socioeconomic status.
Poor sleep patterns and chronic sleep deprivation also contribute.

Alcohol use

Heavy alcohol intake increases BP, triglycerides, and risk of cardiomyopathy and arrhythmias.

Chronic kidney disease (CKD)

Strongly associated with CAD due to disturbances in calcium-phosphate metabolism, inflammation, and shared risk factors.

Inflammatory conditions

Rheumatoid arthritis, lupus, psoriasis, HIV, etc., are associated with increased CAD risk.

Others

Elevated Lp(a), high homocysteine, air pollution exposure.

4. Clinical Features: Signs and Symptoms

The presentation of CAD varies from asymptomatic to sudden death.

4.1 Typical angina

Angina pectoris is chest discomfort due to myocardial ischemia without necrosis.

Characteristics (often summarized as “typical angina”):

Location: Retrosternal, may radiate to left arm, neck, jaw, shoulders, or back.
Quality: Pressure, heaviness, squeezing, tightness, or burning; not usually sharp or localized.
Duration: Typically lasts 2–10 minutes in stable angina; usually less than 20 minutes.
Precipitating factors:

Physical exertion (climbing stairs, walking uphill)
Emotional stress
Cold weather
Heavy meals

Relieving factors:

Rest
Sublingual nitroglycerin within a few minutes

4.2 Stable vs unstable angina

Stable angina:

Predictable pattern of chest pain with a consistent level of exertion or stress.
Relieved by rest or nitroglycerin.
Due to fixed, stable atherosclerotic plaque causing demand-supply mismatch.

Unstable angina (UA):

New-onset angina (less than 2 months) that is severe.
Angina at rest or minimal exertion.
Increasing frequency, severity, or duration (“crescendo angina”).
Part of Acute Coronary Syndrome (ACS), usually due to plaque rupture and partial thrombosis.
No rise in cardiac biomarkers (troponin).

4.3 Myocardial infarction (MI)

STEMI or NSTEMI present with:

Severe, prolonged chest pain (>20 minutes), often more intense and not relieved by rest or nitroglycerin.
May radiate as above.
Associated symptoms:

Shortness of breath
Sweating (diaphoresis)
Nausea, vomiting
Palpitations
Feeling of impending doom
Syncope or near-syncope

4.4 Atypical and silent presentations

Common in elderly, women, and patients with diabetes or chronic kidney disease:

Epigastric discomfort, indigestion-like pain
Isolated dyspnea (shortness of breath)
Fatigue or weakness
Dizziness
Nausea without much chest pain

Silent ischemia: Objective evidence of ischemia (e.g., ECG changes, imaging) without symptoms; common in diabetics because of autonomic neuropathy.

4.5 Physical examination findings

Often normal, especially in stable CAD, but may show:

Tachycardia, hypertension, or hypotension
S3 or S4 heart sounds, new murmur (e.g., papillary muscle dysfunction)
Signs of heart failure: crackles in lungs, peripheral edema, elevated jugular venous pressure
Pallor, cool clammy skin in acute MI
Signs of peripheral vascular disease (diminished pulses, bruits)

5. Investigations

5.1 Initial evaluation

History and physical examination

Character of pain, risk factors, past medical history, family history.

Electrocardiogram (ECG)

At rest and during pain if possible.
May show:

ST depression or elevation
T wave inversion
Pathological Q waves (old MI)

Normal ECG does not rule out CAD.

Cardiac biomarkers

Troponin I or T: highly specific for myocardial necrosis.
Used to differentiate UA (negative troponin) from NSTEMI/STEMI (positive troponin).

Basic blood tests

Complete blood count (CBC)
Serum electrolytes
Renal function tests (BUN, creatinine)
Liver function tests
Fasting blood glucose, HbA1c
Lipid profile (total cholesterol, LDL, HDL, triglycerides)
Coagulation profile (PT, INR, aPTT)

Chest X-ray

Cardiac size, pulmonary congestion, other lung pathology.

5.2 Non-invasive ischemia testing

Exercise stress test (treadmill test)

ECG monitoring during graded exercise.
Detects ECG changes suggestive of ischemia.
Useful in stable CAD with intermediate pre-test probability.

Stress echocardiography

Echocardiogram at rest and during stress (exercise or pharmacologic).
Detects inducible wall motion abnormalities.

Myocardial perfusion imaging (nuclear stress test)

Uses radiotracers (e.g., SPECT, PET) to identify areas with reduced perfusion during stress vs rest.

Stress cardiac MRI

High-quality imaging of perfusion and wall motion.

5.3 Anatomic imaging of coronary arteries

Coronary CT Angiography (CTA)

Non-invasive CT scan with contrast.
Good for ruling out significant CAD in low-to-intermediate risk patients.
Can quantify coronary calcium score.

Invasive Coronary Angiography

Gold standard for defining coronary anatomy.
Catheter inserted (usually via radial or femoral artery), contrast injected; real-time X-ray images taken.
Allows for simultaneous interventional procedures (angioplasty, stent placement).

Intravascular ultrasound (IVUS) and Optical coherence tomography (OCT)

Performed during invasive angiography to assess plaque characteristics and optimize stent placement.

6. Treatment and Management

Management has three main goals:

Relieve symptoms (mainly angina)
Prevent myocardial infarction and death
Improve quality of life and functional capacity

Treatment includes lifestyle modification, pharmacotherapy, and revascularization.

6.1 Lifestyle modification and risk factor control

Smoking cessation

Strongly recommended; use counseling, nicotine replacement, or medications as appropriate.

Dietary changes

Emphasize fruits, vegetables, whole grains, legumes, nuts, fish.
Limit saturated fats, trans fats, red/processed meats, sugar-sweetened beverages, and excessive salt.
Mediterranean-style diet often recommended.

Physical activity

At least 150 minutes/week of moderate-intensity aerobic activity, if tolerated and cleared by provider.
Resistance training 2–3 times/week.

Weight management

Aim for BMI ~18.5–24.9; focus on central obesity (waist circumference).

Diabetes management

Good glycemic control (e.g., HbA1c target individualized, often ≤7%).
Use of agents with proven CV benefit (SGLT2 inhibitors, GLP-1 agonists) in appropriate patients.

Blood pressure control

Target often <130/80 mmHg (individualized).

Lipid management

High-intensity statins for most patients with established CAD.
Add ezetimibe or PCSK9 inhibitors if LDL remains high.

Stress management

Relaxation techniques, counseling, cognitive-behavioral therapy where needed.

6.2 Pharmacotherapy

For patients with chronic/stable CAD (chronic coronary disease), common medications:

Antiplatelet agents

Aspirin (75–100 mg daily) lifelong, unless contraindicated.
If aspirin contraindicated, clopidogrel can be used.
After stent placement or acute coronary syndrome, dual antiplatelet therapy (DAPT) with aspirin + P2Y12 inhibitor (e.g., clopidogrel, ticagrelor, prasugrel) for a defined period.

Statins

Atorvastatin, rosuvastatin (high-intensity regimens).
Stabilize plaques, reduce LDL, anti-inflammatory effects.

Beta-blockers

Reduce heart rate and contractility, lowering oxygen demand.
First-line for angina and post-MI unless contraindicated.

ACE inhibitors / ARBs

Beneficial in patients with CAD plus hypertension, diabetes, LV dysfunction, or CKD.
Improve endothelial function, reduce remodeling.

Nitrates

Short-acting nitrates (sublingual GTN) for acute angina episodes.
Long-acting nitrates for symptom control in chronic stable angina.
Need nitrate-free interval to prevent tolerance.

Calcium channel blockers (CCBs)

Useful when beta-blockers are contraindicated or insufficient.
Particularly helpful in vasospastic (Prinzmetal) angina.

Ranolazine (where available)

Antianginal agent used when other therapies are inadequate.

Others (depending on comorbidities)

SGLT2 inhibitors, mineralocorticoid receptor antagonists in HF with reduced EF.
Anticoagulation when there is atrial fibrillation or LV thrombus.

6.3 Revascularization

Percutaneous Coronary Intervention (PCI)

Balloon angioplasty with placement of stent (usually drug-eluting).
Indicated in:

Acute STEMI (primary PCI, time-critical)
Some NSTEMI/UA patients
Symptomatic stable CAD with significant stenosis not controlled by medical therapy.

Coronary Artery Bypass Grafting (CABG)

Surgical bypass of blocked arteries using grafts (e.g., internal mammary artery, saphenous vein).
Indicated in:

Left main coronary disease
Triple-vessel disease, especially with LV dysfunction or diabetes
Complex lesions unsuitable for PCI

Cardiac Rehabilitation

Structured program combining exercise training, education, risk-factor modification, and psychosocial support.
Improves survival and quality of life.

7. Nursing Care Plan for CAD

Nursing care focuses on acute management, prevention of complications, rehabilitation, and education. Below is an example of a comprehensive care plan, mainly for a patient with CAD presenting with angina or MI.

7.1 Nursing Assessment

Subjective data:

Description of chest pain:

Onset, location, duration, character, radiation
Precipitating and relieving factors

Associated symptoms:

Dyspnea, diaphoresis, nausea, palpitations, dizziness, anxiety

Past history:

Known CAD, hypertension, diabetes, dyslipidemia
Previous MI, PCI, or CABG

Medication history:

Use of nitrates, beta-blockers, aspirin, statins, anticoagulants

Lifestyle:

Smoking, alcohol, diet, physical activity, stress, sleep pattern

Understanding of disease and previous education

Objective data:

Vital signs:

BP, HR, RR, temperature, oxygen saturation, pain scale

Cardiovascular exam:

Heart sounds, murmurs, S3/S4, signs of HF (edema, JVD)

Respiratory exam:

Breath sounds (crackles, wheezes), work of breathing

Peripheral circulation:

Peripheral pulses, skin color, temperature, capillary refill

ECG monitoring:

ST changes, arrhythmias

Laboratory results:

Troponin, CK-MB, lipid profile, glucose, electrolytes, renal function

Weight, fluid balance, intake/output
Psychological state:

Anxiety, fear, coping mechanisms

7.2 Common Nursing Diagnoses (NANDA-style)

Acute Pain related to myocardial ischemia
Evidenced by chest pain, ECG changes, vital sign changes, verbal reports.
Decreased Cardiac Output related to impaired myocardial function
Evidenced by hypotension, tachycardia, weak pulses, decreased urine output, fatigue.
Activity Intolerance related to imbalance between oxygen supply and demand
Evidenced by dyspnea on exertion, fatigue, ECG changes with activity.
Anxiety related to threat of death, health status change, and unfamiliar environment
Evidenced by restlessness, verbalization of fear, increased vital signs.
Risk for Decreased Tissue Perfusion (cardiac, cerebral, renal, peripheral)
Related to decreased cardiac output and atherosclerotic disease.
Knowledge Deficit related to lack of information about disease process, medications, and lifestyle modifications.

7.3 Planning: Goals and Expected Outcomes

Examples of goals:

Patient’s chest pain will be relieved or reduced to acceptable level (e.g., ≤3/10) within 15–30 minutes of interventions.
Patient will exhibit stable vital signs and signs of adequate cardiac output (BP within target, urine output ≥30 mL/hr, alert mental status).
Patient will tolerate gradually increased activity without significant chest pain or dyspnea.
Patient will verbalize reduced anxiety and demonstrate coping strategies.
Patient and family will verbalize understanding of CAD, medications, and necessary lifestyle changes before discharge.

7.4 Nursing Interventions and Rationales

7.4.1 Managing acute pain (angina/MI)

Interventions:

Assess pain characteristics (PQRST: Provocation, Quality, Region/Radiation, Severity, Time) on admission and during episodes.

Rationale: Helps differentiate cardiac from non-cardiac pain, evaluate severity, and monitor response to treatment.

Monitor vital signs and continuous ECG during pain episodes.

Rationale: Detects hemodynamic instability and ischemic changes, arrhythmias.

Administer prescribed oxygen if indicated (e.g., SpO2 < 90–92% or respiratory distress).

Rationale: Increases oxygen available to ischemic myocardium, though routine use in all patients is no longer recommended without hypoxia.

Administer nitroglycerin as ordered (sublingual or IV).

Rationale: Dilates coronary vessels, decreases preload and myocardial oxygen demand, often relieves ischemic pain.

Administer opioid analgesics (e.g., morphine) if pain persists and is severe, as prescribed.

Rationale: Relieves pain, reduces anxiety, and decreases sympathetic activity, decreasing cardiac workload.

Place patient on bed rest or limited activity during acute pain and early recovery.

Rationale: Reduces myocardial oxygen demand.

Maintain calm environment; stay with patient during severe episodes, provide reassurance.

Rationale: Reduces anxiety-induced catecholamine surge, which can worsen ischemia.

Evaluation:

Pain reduced or resolved, ST changes improved, vital signs stabilized.

7.4.2 Optimizing cardiac output and preventing complications

Interventions:

Monitor hemodynamic status:

Frequent BP, HR, rhythm, respiratory rate, SpO2.
Observe for signs of decreased CO: low BP, oliguria, cold clammy skin, confusion.
Rationale: Early detection of deterioration allows prompt intervention (fluids, medications, advanced support).

Monitor intake and output, daily weight, assess for edema and lung crackles.

Rationale: Evaluates fluid status and risk of heart failure.

Administer prescribed medications:

Beta-blockers, ACE inhibitors, antiplatelets, anticoagulants, statins, diuretics as ordered.
Rationale: Improve myocardial oxygen balance, prevent clot extension, support LV function, reduce remodeling.

Check laboratory results regularly:

Troponin trends, electrolytes (K+, Mg++), renal function.
Rationale: Detect ongoing MI, correct electrolyte imbalances that can cause arrhythmias, adjust drug doses.

Prepare and assist for procedures:

Thrombolysis, PCI, CABG when indicated.
Rationale: Restore coronary blood flow as early as possible.

Post-PCI care:

Monitor puncture site (bleeding, hematoma, swelling).
Check distal pulses, limb color and temperature.
Keep limb immobilized as ordered.
Monitor for chest pain recurrence.
Rationale: Early identification of complications such as bleeding, pseudoaneurysm, acute stent thrombosis.

Post-CABG care (if applicable):

Monitor vital signs, chest tube drainage.
Inspect surgical incisions for infection.
Encourage deep breathing, incentive spirometry, early mobilization.
Rationale: Prevent pulmonary complications, promote healing, and prevent venous thromboembolism.

7.4.3 Managing activity intolerance

Interventions:

Assess baseline activity level and symptoms with minimal exertion.

Rationale: Guides individualized activity progression.

Plan rest periods between activities; assist with ADLs as necessary.

Rationale: Avoids excessive cardiac workload.

Gradually increase activity as tolerated:

Begin with sitting in chair, short walks in room, then hallway, under cardiac monitoring if indicated.
Rationale: Promotes conditioning and prevents deconditioning after bed rest.

Monitor response to activity:

HR, BP, RR, SpO2, presence of chest pain, dyspnea, extreme fatigue.
Stop activity and notify provider if:

Chest pain or significant dyspnea occurs.
Marked increase in HR or BP, or drop in BP.

Rationale: Ensures activity is safe and within patient’s tolerance.

Collaborate with physiotherapy and cardiac rehabilitation team.

Rationale: Structured, supervised exercise improves long-term outcomes.

7.4.4 Reducing anxiety and providing psychosocial support

Interventions:

Assess anxiety level, coping mechanisms, and support systems.

Rationale: Identifies patients at high risk for poor coping and depression.

Provide honest, simple, clear explanations of procedures and treatments.

Rationale: Reduces fear of the unknown and builds trust.

Encourage patient and family to express feelings and ask questions.

Rationale: Facilitates emotional release and promotes coping.

Use relaxation techniques:

Deep breathing, guided imagery, music therapy when appropriate.
Rationale: Reduces sympathetic nervous system activity, improves comfort.

Facilitate family presence within hospital policies.

Rationale: Family support reduces anxiety and promotes a sense of security.

Refer to counseling, social worker, or support groups if needed.

Rationale: Addresses long-term psychological issues, depression, or financial concerns.

7.4.5 Patient and family education (knowledge deficit)

Interventions:

Educate about CAD:

Basic pathophysiology in understandable terms.
Explain difference between stable angina and acute MI warning signs.
Rationale: Increases understanding, enhances compliance.

Teach medication regimen:

Purpose, dose, timing, side effects, importance of adherence.
Specifically instruct on:

Proper use of nitroglycerin (how and when to take, max doses before seeking help).
Lifelong antiplatelet therapy indications.

Rationale: Ensures safe and effective use of medications.

Discuss lifestyle modifications:

Smoking cessation strategies.
Dietary recommendations (low saturated fat, low sodium, high fiber, adequate fruits/vegetables).
Importance of regular physical activity and weight control.
Rationale: Addresses modifiable risk factors; reduces recurrence.

Explain cardiac rehabilitation and encourage participation.

Rationale: Structured program improves outcomes and quality of life.

Teach when to seek immediate medical help:

New or worsening chest pain not relieved by rest or nitroglycerin.
Shortness of breath, syncope, palpitations, signs of heart failure.
Rationale: Promotes early recognition of complications and rapid treatment.

Provide written materials and verify understanding using teach-back method.

Rationale: Reinforces verbal teaching and ensures accurate comprehension.

7.5 Evaluation

Nursing care is evaluated continuously. Desired outcomes:

Pain is effectively controlled; patient reports acceptable comfort level.
Vital signs and hemodynamic parameters remain stable.
Patient engages in progressively increased activity without significant symptoms.
Patient demonstrates reduced anxiety, verbalizes coping strategies.
No major complications (e.g., reinfarction, HF, arrhythmia, bleeding).
Patient and family can accurately describe:

Nature of CAD
Medications and their purposes
Lifestyle changes required
When and how to seek emergency help

NURSING CARE PLAN – CORONARY ARTERY DISEASE (CAD)

Assessment	Nursing Diagnosis	Goals / Expected Outcomes	Nursing Interventions	Rationale	Evaluation
Chest pain, tightness, radiation to left arm, jaw	Acute Pain related to decreased myocardial blood flow	Patient will report reduced chest pain	- Assess pain (location, severity, duration) - Administer prescribed analgesics and nitrates - Provide oxygen therapy - Maintain bed rest	Reduces myocardial oxygen demand and relieves ischemia	Pain reduced / relieved
Shortness of breath, low SpO₂	Impaired Gas Exchange related to reduced cardiac output	Patient will maintain adequate oxygenation	- Monitor SpO₂ - Administer oxygen - Position patient in semi-Fowler’s position	Improves lung expansion and oxygen delivery	SpO₂ within normal range
Increased BP, weak pulse, fatigue	Decreased Cardiac Output related to impaired myocardial contractility	Maintain adequate cardiac output	- Monitor vital signs and ECG - Observe for arrhythmias - Administer cardiac drugs as prescribed	Early detection prevents complications	Stable vital signs
Anxiety, restlessness, fear of death	Anxiety related to chest pain and fear of complications	Anxiety level will be reduced	- Provide reassurance - Explain procedures and condition - Encourage verbalization of feelings	Reduces stress and oxygen demand	Patient appears calm
Sedentary lifestyle, poor diet history	Ineffective Health Maintenance related to lack of knowledge	Patient will adopt healthy lifestyle practices	- Educate about CAD and risk factors - Advise low-fat, low-salt diet - Encourage regular exercise - Counsel smoking cessation	Prevents disease progression	Patient verbalizes understanding
Fatigue, weakness	Activity Intolerance related to imbalance between oxygen supply and demand	Patient will tolerate activity without symptoms	- Gradually increase activity - Monitor response to activity - Provide rest periods	Prevents overexertion	Activity tolerated

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Comprehensive Guide to Coronary Artery Disease (CAD) for Nursing and Health Students : Nursing Care Plan:

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